در هنگام جستجو کلمه در قسمت عنوان میتوانید کلمات مورد جستجو را با کاراکتر (-) جدا کنید.
کاربرد نوع شرط:
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Inflammation,Fibrosis,Akt,Myocarditis,Deguelin
- چکیده:
- چکیده انگلیسی: Objective(s): Myocarditis is characterized by inflammatory cell infiltration in myocardial stroma. Attenuation of tumor necrosis factor (TNF)-α and interleukin (IL)-1β is a reliable mark for improving the prognosis. Protein kinase B (Akt) plays an important role in the development and progression of myocarditis. The specific role of the natural inhibitor of Akt, Deguelin, on myocarditis has not been reported. In this study, we used deguelin to investigate the effects of natural Akt inhibitor on myocarditis in experimental autoimmune myocarditis (EAM) rats.
Materials and Methods: EAM rat models were made by using Lewis rats and Deguelin was injected intraperitoneally on day 3, 6, 9, 12 and 15 after successful modeling. On day 18, rats were sacrificed and the heart weight (HW)/ body weight (BW) ratio were measured. The pathological changes, pathological scores and fibrosis area were evaluated after H.&E. and Masson’s trichrome staining. The mRNA levels of TNF-α and IL-1β were measured by RT-qPCR, while the protein expressions of TNF-α and IL-1β were detected by immunohistochemical staining and Western bolt. The protein expressions of Akt, Akt1, phosphorylated (p-) Akt and nuclear factor (NF)-κB were detected by Western bolt.
Results: We found that the TNF-α and IL-1β levels, inflammatory scores and fibrosis areas were markedly increased after 18 days deguelin administration.
Conclusion: Akt inhibition with deguelin may aggravate myocarditis of EAM rats.- انتشار مقاله: 21-07-1397
- نویسندگان: Shanshan Li,Yue Wang,Chunming Zhao,Meixiang Zhang,Wei Wang,Xiaowei Yu,Jiao Huang,Zhao Wang,Bo Zhu,Cheng Qian Yin,Hongxing Cai
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Inflammation,Fibrosis,Akt,Myocarditis,Deguelin
- چکیده:
- چکیده انگلیسی: Objective(s): Myocarditis is characterized by inflammatory cell infiltration in myocardial stroma. Attenuation of tumor necrosis factor (TNF)-α and interleukin (IL)-1β is a reliable mark for improving the prognosis. Protein kinase B (Akt) plays an important role in the development and progression of myocarditis. The specific role of the natural inhibitor of Akt, Deguelin, on myocarditis has not been reported. In this study, we used deguelin to investigate the effects of natural Akt inhibitor on myocarditis in experimental autoimmune myocarditis (EAM) rats.
Materials and Methods: EAM rat models were made by using Lewis rats and Deguelin was injected intraperitoneally on day 3, 6, 9, 12 and 15 after successful modeling. On day 18, rats were sacrificed and the heart weight (HW)/ body weight (BW) ratio were measured. The pathological changes, pathological scores and fibrosis area were evaluated after H.&E. and Masson’s trichrome staining. The mRNA levels of TNF-α and IL-1β were measured by RT-qPCR, while the protein expressions of TNF-α and IL-1β were detected by immunohistochemical staining and Western bolt. The protein expressions of Akt, Akt1, phosphorylated (p-) Akt and nuclear factor (NF)-κB were detected by Western bolt.
Results: We found that the TNF-α and IL-1β levels, inflammatory scores and fibrosis areas were markedly increased after 18 days deguelin administration.
Conclusion: Akt inhibition with deguelin may aggravate myocarditis of EAM rats.- انتشار مقاله: 21-07-1397
- نویسندگان: Shanshan Li,Yue Wang,Chunming Zhao,Meixiang Zhang,Wei Wang,Xiaowei Yu,Jiao Huang,Zhao Wang,Bo Zhu,Cheng Qian Yin,Hongxing Cai
- مشاهده
- جایگاه : پژوهشی
- مجله: Asian Pacific Journal of Cancer Prevention
- نوع مقاله: Journal Article
- کلمات کلیدی: Lung cancer,Meta-Analysis,Polymorphism,matrix metalloproteinase1 (MMP1)
- چکیده:
- چکیده انگلیسی: Objective: The association between matrix metalloproteinase1 (MMP1)-1607 1G>2G polymorphism and lung cancer
risk is still inconclusive and inconsistent. We conducted a meta-analysis to estimate the potential relationship between
MMP1-1607 1G>2G polymorphism and lung cancer risk. Methods: The comprehensive searches of the PubMed, Web
of Science, Medline, CBM, CNKI, Weipu, and Wanfang databases, published up to Nov 10, 2018. Statistical analyses
were performed with Review Manager 5.3 software. Results: A total of 14 relevant studies containing 6068 cases and
5860 controls were included in the study. The results indicated that MMP1-1607 1G>2G polymorphism was significantly
associated with increased lung cancer risk under four models: 2G vs. 1G model (pooled OR = 1.19, 95% CI = 1.05-1.34,
P < 0.0001); 2G/2G vs. 1G/1G (pooled OR = 1.34, 95% CI = 1.09-1.64, P = 0.003); 2G/2G vs. 1G/1G+1G/2G (pooled
OR = 1.26, 95% CI = 1.06-1.49, P < 0.0001); 2G/2G+1G/2G vs. 1G/1G (pooled OR = 1.21, 95% CI = 1.05-1.40, P
= 0.01). Subgroup analyses showed that there was a higher increase in smoking status under three models: 2G/2G
vs. 1G/1G (pooled OR = 2.07, 95% CI = 1.14-3.77, P = 0.02); 2G/2G vs. 1G/1G+1G/2G (pooled OR = 1.71, 95% CI
= 1.17-2.52, P = 0.006); 2G/2G+1G/2G vs. 1G/1G (pooled OR = 2.03, 95% CI = 1.14-3.62, P = 0.02). In addition,
subgroup analyses by ethnicity further identified the significant association in Asians. Non-smoking population and
ethnicity among Caucasian had no relationship with lung cancer susceptibility in four models. Conclusion: Our study
suggested that MMP1-1607 1G>2G polymorphism was a risk factor for developing lung cancer risk.- انتشار مقاله: 11-11-1397
- نویسندگان: Yue Ma,Xi Yang,Yu-Ping Xie,Cheng Yi,Fen Zhao,Ying Huang
- مشاهده